The studies on cerebral ischemia, its pathophysiology, prevention and therapy in gerbils have been concerned with continuous evaluation of the effects of naturally occurring central nervous system depressant [-butyrolactone (GBL) and -hydroxybutyrate (GHB)] on cerebral ischemia focusing on the elucidation of the possible mechanisms responsible for the observed beneficial effect of GBL and GBH on ischemic brain edema. These investigations showed that the postischemic GHB treatment 3 hours after release of bilateral carotid occlusion GHB reverses the observed increased turnover time and decreased turnover rate (decreased 5-HT release and synthesis) at 4 hours reflow after the ischemic insult in the cortex hippocampus and partly in the striatum. However, 5-HIAA accumulation is unaffected by GHB treatment. These results suggest that the reported beneficial manifestations of the postischemic GHB treatment may be related to 5-HT synthesis which appears to be enhanced in the treated as compared to the untreated ischemic animals. These findings also indicate that the postischemic GHB treatment stabilizes the ischemically disturbed serotonin metabolism. Therefore, the observed short term improvement in one of monoamines metabolism following a relatively late post-ischemic treatment warrants further studies of GHB as a potential therapeutic agent in cerebral ischemia.